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Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;46(9): 746-751, 19/set. 2013. graf
Artigo em Inglês | LILACS | ID: lil-686569

RESUMO

Macrophage migration inhibitory factor (MIF), a pleiotropic cytokine, plays an important role in the pathogenesis of atrial fibrillation; however, the upstream regulation of MIF in atrial myocytes remains unclear. In the present study, we investigated whether and how MIF is regulated in response to the renin-angiotensin system and oxidative stress in atrium myocytes (HL-1 cells). MIF protein and mRNA levels in HL-1 cells were assayed using immunofluorescence, real-time PCR, and Western blot. The result indicated that MIF was expressed in the cytoplasm of HL-1 cells. Hydrogen peroxide (H2O2), but not angiotensin II, stimulated MIF expression in HL-1 cells. H2O2-induced MIF protein and gene levels increased in a dose-dependent manner and were completely abolished in the presence of catalase. H2O2-induced MIF production was completely inhibited by tyrosine kinase inhibitors genistein and PP1, as well as by protein kinase C (PKC) inhibitor GF109203X, suggesting that redox-sensitive MIF production is mediated through tyrosine kinase and PKC-dependent mechanisms in HL-1 cells. These results suggest that MIF is upregulated by HL-1 cells in response to redox stress, probably by the activation of Src and PKC.


Assuntos
Animais , Camundongos , Peróxido de Hidrogênio/farmacologia , Oxirredutases Intramoleculares/efeitos dos fármacos , Fatores Inibidores da Migração de Macrófagos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Oxidantes/farmacologia , Proteína Quinase C/metabolismo , Quinases da Família src/metabolismo , Angiotensina II/metabolismo , Western Blotting , Linhagem Celular , Imuno-Histoquímica , Oxirredutases Intramoleculares/genética , Microscopia Confocal , Fatores Inibidores da Migração de Macrófagos/genética , Estresse Oxidativo/fisiologia , Inibidores de Proteínas Quinases/farmacologia , Reação em Cadeia da Polimerase em Tempo Real , Sistema Renina-Angiotensina/fisiologia
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